Bile functions as the body’s emulsifying agent, critical for fat digestion and assimilation. Bile is produced by the liver, and it is temporarily stored in the gall bladder. Bile is released into the small intestine in response to hormones, such as cholecystokinin, when fat enters the intestine.

Electroplytes are present at levels found in serum. The ratios of in-dividual lipids are critical to maintain a stable micellar liquid. The molar ratios are typically 5:15:80 for cholesterol/phospha-tidylcholine/bile salts. If the bile concentration becomes too high, cholesterol will precipitate and gallstones will form in the gall bladder, a condition known as cholelithiasis (1).

Bile formation

Bile salts and acids represent oxidized derivatives of cholesterol. About 80% of the cholesterol in the body will eventually be disposed of as cholic acid. The primary bile acids, cholic acid and chenodeoxycholic acid, possess a carboxylic acid side chain, which confers hydrophilic properties to the lipophilic sterol ring and creates detergentlike molecules. The liver attaches taurine and glycine to bile acids to create bile salts (taurocholate or taurochenodeoxycholate, and glycocholate or glycodeoxycholate, respectively). Bacterial enzymes in the colon can convert these to secondary bile acids, deoxycholate and lithocholate.

Bile and digestion

Bile is needed for efficient uptake of oily nutrients. When bile acids and bile salts first encounter ingested fats, they act as emulsifiers to create suspensions which can be broken down enzymatically. The process involves several important steps:

1. The combined action of bile salts and pancreatic lipase initiates hydrolysis of triglycerides to free fatty acids and diglycerides with the formation of emulsions containing other lipid-soluble nutrients, including vitamins and carotenoids. The particle size of these emulsions ranges from 200 to 5000 nm in diameter.

2. Lipase is then able to hydrolyze di-and triglycerides to monoglycerides and free fatty acids. Lipase requires a smaller protein called colipase, another pancreatic product, in order to bind to triglycerides and activate the lipase.

3. Upon further release of bile salts, the lipid aggregates become smaller, from 3 to 10 nm in diameter. The normal endpoint of triglyceride digestion is a product containing 70% free fatty acid anions, and 25% beta monoglycerides, together with cholesterol. The micelles are taken up by epithelial cells of the brush border by passive diffusion. After absorption, the fate of fatty acids depends upon their sizes. Medium chain fatty acids, with less than 10-12 carbons, pass directly from the mucosal cells into the portal blood and bind to serum albumin. Longer chain fatty acid anions are re-esterified with beta monoglycerides in the smooth endoplasmic reticulum to reform triglycerides. The newly synthesized triglycerides are then complexed with apoproteins, cholesterol and phospholipids, to produce particles called chylomicrons. These particles are released from mucosal cells by exocytosis and enter the lymph, rather than entering the bloodstream directly.

Enterohepatic circulation

Bile salts do not cross the mucosal barrier into the lymphatic system, but rather they are reabsorbed as micelles in the lower region of the small intestine. Most of the bile salts released into the intestine are reabsorbed in the lower ileum where bacteria can reduce free bile acids to lithocholate and deoxycholate. The absorbed bile acids and salts are transported via the portal vein to the liver as complexes with serum albumin. The liver efficiently extracts them, conjugates them with amino acids, and again secretes them as bile, which is returned to the gall bladder to continue to aid digestion. Bile salts recirculate 2-3 times through the liver with each meal.

Betaine

Beets contain high amounts of Betaine which is used to add a methyl group to Homocysteine and thus form Methionine and Dimethylglycine. Dimethylglycines is a methyl-donor that helps in the detoxification and immune system pathways. In one study, after exposure to carbon tetrachloride (CC14), there was a reduction in liver necrosis and a significant reduction in liver damage after oral treatment of betaine (2). Another study showed that after injection of CC14 to test animals, supplemental betaine reduced triglyceride in the liver and centrilobular hepatic lipidosis induced by the CC14 injections (3).

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